ArticleIbrain2021
The expanded effects of sevoflurane on the nervous system: the harmful effect of residual concentration of sevoflurane on the respiratory system through neurogenic inflammation.
Article in Ibrain, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed, 2 citations in OpenAlex.
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Authors and funding
9 authors at 1 institution in 1 country.
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Abstract
Background: Neurogenic inflammation caused by sevoflurane may not only limite to the nervous system, but also expand to the respiratory system. The purpose of this study was to investigate the expression changes of transient receptor potential vanilloid 1 (TRPV1), neurokinin A (NKA), neurokinin B (NKB), calcitonin gene related peptide (CGRP) and substance P (SP) in 14, 21 and 42-day-old rats after inhaling 0.4% sevoflurane, in order to evaluate whether the residual sevoflurane be harmful to the respiratory system through neurogenic inflammation. Methods: The anesthetic inhalation device was designed to allow 14, 21 and 42-day-old rats inhale 0.4% sevoflurane, while rats in the control group inhaled 40% O Results: After inhaling 0.4% sevoflurane, the expression of TRPV1 in lung tissue of 14 and 21-day-old rats was significantly higher than that of the control group, as well as increased the expression of CGRP and SP in the trachea of 14-day-old rats and NKA, NKB, CGRP and SP in the trachea of 21-day-old rats. CPZ pretreatment could antagonize these effects. Conclusion: Residual sevoflurane during resuscitation of inhalation anesthesia could induce neurogenic inflammation by activating TRPV1, which damaged to the developing respiratory system, but has no significant effect on the respiratory system in adulthood.
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